Primary resistance exists in cancer cells that are not addicted to oncogenic KRAS signals.[11, 12] For pan‐KRAS inhibitors working by interrupting the nucleotide exchange, primary resistance exists in tumors driven by KRAS G12R and Q61R/K/L.[10] These mutants are activated by the damaged GTP hydrolysis instead of the increased nucleotide exchange. This evidence concerns the gene KRAS and cancer.